Lipid-lowering drugs Flashcards

1
Q

when should lipid lowering therapy be offered?

A

For primary prevention of CVD in people:

  • aged <84 if QRISK assessment >=10%
  • T2DM + other CVD risk factors
  • T1DM
  • CKD
  • familial hypercholesterolaemia
  • consider offering if age >=85

For secondary prevention of CVD in adults with established CVD, e.g. past or current Hx of MI, angina, stroke, TIA or PAD.

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2
Q

which investigations should be performed before initiation treatment?

A
  1. Full lipid profile: total cholesterol, HDL and non-HDL cholesterol and triglycerides
  2. LFTs - contraindicated in active liver disease
  3. renal function tests - dose adjustments required in CKD
  4. HbA1c - to Dx possible DM
  5. TSH - hypothyroidism is recognised cause of dyslipidaemia and untreated hypothyroidism increases risk of statin induced myopathy
  6. if pt has generalised unexplained muscle pain, measure CK levels - if 5x or more upper limit of normal, re-measure after 7 days; if still high, seek specialist advice.
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3
Q

which lipid modification therapies would you offer for primary and secondary prevention of CVD?

A
  1. Primary prevention:
    - 1st line: 20 mg ATORVASTATIN - aim for >40% reduction in baseline non-HDL cholesterol
    - 2nd line: reinforce adherence to lifestyle changes, consider increasing dose and if target still not achieved, consider co-prescription of EZETIMIBE in pts with primary hypercholesterolaemia
  2. Secondary prevention: 80 mg ATORVASTATIN
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4
Q

what is the MOA of statins?

A

Inhibit HMG CoA reductase… decreased hepatic cholesterol synthesis.

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5
Q

suggest characteristic ADRs of statins

A
  1. myopathy: inc. myalgia, myositis, rhabdomyolysis and asymptomatic raised CK
  2. liver impairment: check LFTs at baseline, 3 mths and 12 mths (discontinue if ALT/AST rise to and persist 1 3x upper limit of reference range
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6
Q

what time of day should statins be taken?

A

At night as time is when majority of cholesterol synthesis takes place.

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7
Q

what is the MOA of ezetimibe?

A

inhibits cholesterol Rs on enterocytes, inhibition absorption from small intestine

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